When Eric Hipple quarterbacked the Detroit Lions in the 1980s, he figures he took at least one shot to the head every time he played. “You get tackled, you get hit, your head bounces–so if nothing else, you see stars … I can seriously say that by the standards they use today, I was concussed at least every game that I played in.”

There’s a video on YouTube that shows Hipple being torpedoed so hard he loses his helmet, and his unprotected head bounces several times. It’s scarily easy, as you watch it, to imagine Hipple ending up like former Atlanta Falcons safety Ray Easterling, who shot himself in April while suffering from dementia and depression. An autopsy found evidence of chronic traumatic encephalopathy (CTE), a degenerative brain disease caused by repeated head injuries. Former San Diego Chargers linebacker Junior Seau shot himself just two weeks later–like Easterling and former Chicago Bear Dave Duerson last year, in the chest rather than the head. In a final text message, Duerson asked his family to send his brain to a research group based at Boston University that studies CTE; they found damage in his.

Easterling’s widow is continuing to pursue the class action suit he filed against the NFL, claiming that the league concealed links between playing football and suffering brain injuries. His and others’ deaths–and lawsuits–are causing ripples everywhere from high school football and hockey teams to soccer programs. But as Hipple sees it, the trouble began long ago.

As outreach specialist for the U-M Depression Center, Hipple works in a windowless office at the East Medical Campus on Plymouth Rd. “There is a group of guinea pigs who were taught the game of football and given a really, really hard object on their heads, called a helmet, to protect their heads,” he says. “But it turned out to be a better weapon than just protection, and nobody told them what the effects of banging your head every day would be … There wasn’t much research being done by the NFL, or by the helmet company, or by anybody else.”

Rather than protecting the players, he says, the league’s concern was, “‘the game goes forward–we’re protecting that.'”

After he left the Lions in 1989, Hipple started a successful insurance business. But in 2000, when his son Jeff killed himself, his world imploded. When Hipple was jailed for DUI, he realized he needed to understand what could drive a fifteen-year-old to suicide.

At the time, Hipple told the [Salt Lake] Deseret News, “I had never heard of depression.” It wasn’t until 2002, when he participated in an eight-week program at the U-M Depression Center, that he realized that Jeff had shown classic symptoms of the disease–and that he himself had them, too.

Men of Hipple’s generation–especially macho football players–rarely talked about depression. Reinventing himself as an advocate for recognizing and treating depression, he was so effective as a volunteer that Depression Center executive director John Greden hired him. He speaks to, among others, former military service members and retired NFL players about depression, resilience, and suicide prevention.

About five years ago, Hipple took part in a study of NFL players. “It was called ‘Pain and Depression in NFL Football,'” he recalls. When it came out, the media focused on the finding that “about 40 percent of former NFL players complain of chronic pain.” What stood out for Hipple and his colleagues, though, was that 15 percent of the ex-players reported suffering from depression.

“So we started a program here [at the Depression Center] to bring more players in.” Then, in a study conducted for the NFL by the U-M’s Institute for Social Research, former players reported rates of early-onset dementia that were nineteen times higher than the general population’s. “Then the CTE [news] broke–that came out of Boston University. Then boom. It exploded.”

Guys who prided themselves on their toughness could tell themselves, in Hipple’s words, “I don’t suffer from a mental illness. I am suffering from the fact that I played football and I hit my head a lot.”

Among ex-players, those findings “kind of shifted [attention] away from depressive illnesses that everybody has, to ‘This is just us,'” Hipple says. “Yet that’s probably not the case … The [physical] loss that goes along with this career,” and the sudden plunge into obscurity that follows it, “really sets a person up for depression and mood disorders.”

To Hipple, getting people diagnosed and treated is the most important thing, and if they find it easier to come in if they think their symptoms are caused by contact sports, “it really doesn’t matter. We’re all trying to treat the symptoms.”

Just since the NFL season began, Hipple has started working with five more players. But he is well aware that equating concussions with depression and dementia vastly oversimplifies the ways in which genetics, life experience, and contact sports interact to affect mental health.

“Here is the unique place I find myself,” he says. “I understand as a player that there was a lot of risk [in professional football] … But I also lost my son, who never played football, never hit his head, never used any drugs, or anything–and yet died from depression.

“So for me, I know that world [of depression as a disease] is real. If that hadn’t happened, I might be falling into the category of ‘Yeah, that’s what happened. I hit my head. That’s why I feel that way.’ Somewhere in the middle is where we all meet.”

Neurologist Jeffrey Kutcher started the U-M’s Neuro-Sport program seven years ago to bridge the gap between primary care and sports medicine. He says that many people underestimate the connection between neuroscience and sports injuries, and overestimate the training and expertise of primary care physicians and pediatricians who are trying to answer the questions of parents whose children are playing aggressive contact sports–many starting at age nine.

Like Hipple, Kutcher is seeing a surge in concern about the long-term effects of athletic head injuries. “Concussion study continues to gain steam and energy and importance, which is all good,” says Kutcher, sitting in the Plymouth Rd. Sweetwaters, near his office in Domino’s Farms. “Our program has grown clinically, for sure. We see a lot of local folks. More and more national referrals come in from professional athletes–both current athletes who have been injured and are having a hard time coming back, [and] former athletes who are concerned about symptoms they may be having and what it means for their long-term health. We are helping a lot of athletes make retirement decisions–should they continue to play or not decisions.”

In its last fiscal year, NeuroSport’s doctors saw about 1,000 patients. Kutcher says that half that number were high schoolers from around southeast Michigan. Twenty percent were college players, active and retired pros 15 percent, and youths as young as nine the final 15 percent.

“A lot of them just got concussed last week [and want to know] ‘When do I go back?’ I’m helping them with their return-to-play decision. That’s fairly common. The next level would be this: ‘It’s the third one [concussion] I’ve had in three months. My coach says I can’t play anymore.’ There’s the ‘I was concussed six months ago, and I’m still having headaches’ person.

“Those cases are interesting because they are always, always, always more complex than people realize. It’s very rarely just concussion. Concussion opens up or magnifies all kinds of pre-existing situations. … It is not concussion that is the problem. It’s head trauma that is the problem. It’s a nuance, but it’s a very, very important one.

“A concussion is the clinical syndrome that is produced by a hit or a series of hits [and] that includes, over the next few days, you feel lousy, you have a headache, you have whatever else. That’s a concussion. The long-term consequences are probably not linked to what produced the [concussion] syndrome at the time, but how much overall force your brain has seen over your life.”

But, he adds, “not every brain injury causes symptoms. As a neurologist I understand that. You name the process–stroke, MS, cancer, whatever–you can have a certain amount of it in your brain and not have a clinical effect.

“So why should we expect that every perturbation of physiology based on a force is going to cause a symptom complex? We’re looking at concussion as a symptom complex. The key part is that every brain has a different threshold for absorbing force before it produces injury, and for having a certain amount of injury before it produces symptoms. There is no way of telling that ahead of time, except [through an individual’s] history.”

Kutcher gives an example. “A fifteen-year-old high school kid had his fifth concussion playing hockey, and he wants to play the rest of his years in high school. Is it safe to do so? His history basically revealed that he has had a consistent problem with headaches that are migraine, and his family has a history of migraines. And those brains that produce migraines are really good at producing symptoms, because they do so at baseline sometimes for no real good reason.

“His concussions were all short-lived–a few hours’ headaches, after a hit, that went away. So five concussions in him? In the sea of the other thirty migraine headaches he’s had in the season? Five concussions, in him, [is] not a huge deal to me.

“Someone who comes in with a different story–of five episodes of head trauma that caused ten days of symptoms the first time, two weeks the next time, or more, symptomatically diverse, and he didn’t have a history of migraine–that’s a different story. That’s somebody I’m worried about.”

Not understanding that variability, some athletes may be worrying needlessly, even dangerously. “This past month I’ve had three ex-professional athletes–two ex-NHL players, one ex-NFL player–come to me essentially with their chief complaint: ‘I don’t want to kill myself.’

The NFL suicides “got them to come see me, which is awesome,” Kutcher says. “But what I’m worried about are the ones who aren’t coming to see me. There is a very well-known concept of suicide contagion.”

In any group, he explains, a certain number of people will be depressed and at risk of suicide. And publicity about the suicide of one member of a group has been shown to cause “a documented increase in suicides in the population that is being reported about.”

That, he believes, “is exactly what’s going on” with the recent deaths of pro football players.

The risk is magnified when people oversimplify–for instance, if they assume that because the Boston study found evidence of CTE in some players’ brains, everyone who ever played contact sports is doomed to suffer depression or dementia.

“The Boston University folks have set up a center looking specifically at CTE,” Kutcher notes. “They have collected the brains of contact sport athletes who in most cases have had some problems. They are collecting a case series. There is a very natural bias in there. They understand that. You can’t base any kind of risk estimate on a collection of cases. You have to look at a population and study risk factors and what the critical outcomes are.

“The problem is, their message gets misunderstood very easily. So I am really concerned that the Boston University group’s message of suicide risk in athletes … is driving people to commit suicide.”

While Eric Hipple gets people into treatment and Jeff Kutcher assesses their cognitive states, Hank Paulson is trying to untangle the physiology of brain damage.

Paulson, director of the Michigan Alzheimer’s Disease Center, works in a windowed corner office in the Biomedical Science Research Building, at the bend where Huron and Washtenaw meet. He sees patients no younger than fifty, and though he doesn’t work at NeuroSport, some of his patients, too, are former sports greats. What he does is “in the family” of CTE, he says, but he deals less with what’s “in the news” and more with what anyone who simply grows old might have to cope with.

“There are a lot of things that are critical to the makeup of a cell,” explains Paulson. “Lipids, DNA, RNA, proteins. Proteins are essentially ribbons of amino acids … it would be similar to beads on a necklace, but in the cell there are very few proteins that look like a necklace. Instead, they clump into specific shapes.

“There is a probability for any given newly made protein to mis-fold–that is, to not take the right shape. You might have some of the beads inside sticking out [of the correct shape]. They might be hydrophobic, stick to membranes, stick to fats–they might tend to lead to clumping of the proteins.” This clumping occurs all the time in degenerative brain diseases like Alzheimer’s, Parkinson’s, and, to some extent, CTE.

“In CTE the key protein is called tau,” Paulson says. “Alzheimer’s disease itself is due to the abnormal accumulation of, and the consequences of, both beta amyloid and tau … You can’t have just one [of those] and be Alzheimer’s.” So why is the Boston study finding only tau in football players’ brains? “We don’t know the answer to that,” Paulson says.

“When I talk about CTE, I’m not talking just about pro football players,” Paulson stresses. “I’m talking about people in car accidents, people from the battlefield–veterans who have suffered a concussion–boxers. One of the key mysteries is what is the connection, if anything, between the early amyloid and the later tau? What is the connection between the amyloid, which occurs outside cells for the most part, and the tau, which occurs inside the cells? They are both vitally important to develop the disease.

“We haven’t figured that connection out very well,” Paulsen acknowledges. But “if you identify that connection, there might be a target for therapy.”

Paulson explains that Alzheimer’s can be diagnosed definitively only at death, when an autopsy finds amyloid and tau in the brain. But “there is a spinal fluid test which measures both amyloid and tau, and can help to determine whether someone has Alzheimer’s or not.”

Presumably, the same markers could help identify CTE. But over at NeuroSport, they don’t use the spinal fluid test. Kutcher, who works with both the U-M and EMU athletic departments, explains that before they compete, every player in every sport “gets a full history and physical evaluation … But then for the contact sport athletes–football, hockey, wrestling, water polo, etc.–we do special baseline testing.” Those cognitive and other tests allow the physicians to assess any loss in function when a player is hurt.

So why not test patient’s spinal fluid for tau, too? “The main reason is, we have no idea what it means,” Kutcher says. “We really don’t.” Everyone has some tau in the brain, he points out–it’s when it “shows up in increased amounts in a certain pattern that has been indicative of disease. At autopsy there is a pattern of tau in the brain that has had a common link of multiple head injuries, or head impacts.

“What we don’t know is what does that mean clinically in a living person. There are examples of hockey players and football players and other people who have died who have had tau in their brain and been labeled by pathologists as having CTE, who [had] no neurological symptoms at all. So if I’m going to go screen for tau in people, I want to know what it means.

“If we had that part of the equation set out that said tau causes dysfunction by doing this in the neuron, and it takes this amount of tau, this amount of distribution, to cause depression and that kind of stuff over time–if we had that, then you could say, ‘Yeah, [let’s test everyone].’ That amount of tau would be like screening for diabetes [by seeing] if someone’s blood sugar was high.” But, he says, “we don’t have that.”

The uncertainty makes it harder to reassure players, and their families, who worry about the long-term repercussions of playing contact sports–especially since some really do have cause for concern. “Absolutely, I’ve had cases where [I’ve had to say to a patient], ‘I think head trauma is causing a change in your brain function. I don’t think you should play anymore,'” Kutcher says. “It’s less common than my saying, ‘There are a lot of other reasons for your symptoms. Let’s move forward with a [treatment] plan.'”

Kutcher says that he and Eric Hipple “are very close.” Hipple went through the full NeuroSport workup, and all his tests came back fine. His head was damaged for sure, and he has problems sleeping, but he always has had. He’s already arranged to have his brain donated to the Boston study, but he didn’t have his tau tested.

Hipple recognizes that his depression predated those hard hits on the football field, and that his and other retired players’ struggles often are as much psychological as physical. Overnight, they go from being stars to nobodies, losing their support systems, their income, even their identities. “It’s traumatic,” he says. Even so, given the choice, he says, he’d do it all again.

But the risk a person is willing to take himself, and the risk he’s willing to see his child take, are often very different. Football made New England Patriots (and former U-M) quarterback Tom Brady rich and famous–yet earlier this year, his dad was quoted as saying that if he had known then what he knows now, he might not have encouraged his now multi-millionaire son to play pro football.

“I don’t know if I’d let my son play,” Hipple concurs. Making it to the pros, he says, “is a pretty cool experience. But there’s a lot of stuff that happens to you. You don’t know if you’d wish that on your enemy.”

But Hipple doesn’t believe the future necessarily has to repeat the past–or that awareneses of the risk of CTE will spell the end of his sport. “I think rule changes will happen in football,” he says. “I think right now it is inevitable … And that is not a bad thing.

“When they moved the goal posts out of the end zone–you look back at that now and you say, ‘that looked like a really smart thing to do.’ But why did they have them in the end zone, when people were running into them?

“Ten years from now we will say, it’s a wonderful game, and those rule changes were necessary.”