ANN ARBOR, Mich. – We were in a coffee shop not far from his office at the University of Michigan when Jeffrey Kutcher tried to explain his concerns in a way I could easily understand.
Kutcher, an associate professor at Michigan, is the chair of the Sports Neurology Section of the American Academy of Neurology and a consultant to the NHL Players' Association. He has been on the fall tour with NHLPA executive director Don Fehr educating players about concussions. And he has an issue with the way Boston University's research on chronic traumatic encephalopathy has been presented to the public.
I want to share our exchange – and BU's response – as a companion to my report on the issue to illustrate the debate further. Kutcher began by referring to abnormal deposits of tau protein in the brain that signal CTE.
"You're describing pathological changes in the brain that may or may not have a clinical relevance," Kutcher said, before turning the tables on me in our interview. "Do you have heart disease?"
"Not that I know of," I said.
"Do you have atherosclerosis?"
"Not that I know of."
"Yes, you do. Everybody does. You have some. If I cut open your heart vessels, I'm going to find [atherosclerosis] in your heart vessels."
"With my diet, I'm sure you would," I responded, trying to make a joke.
"Anybody your age," Kutcher said, still serious. "Do you have heart disease?"
"I guess I do."
"Nah," Kutcher said, meaning not necessarily. "You can live to 80 with that and not have a problem. So they're finding changes in the brain that are described across ages and situations and saying, 'Aha, CTE!' I would say, 'Aha, tau deposition in the brain!' Where's the encephalopathy part? Where's the sick brain part?"
Basically, Kutcher is saying the black stuff that BU researchers have found in the brains of deceased athletes does not necessarily indicate a problem that would affect a person's life. BU diagnosed former NHL player Rick Martin with CTE, but his disease was in the second of four stages. He died of a heart attack in March at age 59. He had no outward symptoms of CTE.
"When they say Rick Martin had Stage 2 CTE, that was just a description of the stuff in the brain," Kutcher said. "He had no clinical problems at all, which goes back to what I said about – do you have plaque or do you have heart disease? … Everybody gets plaque in their arteries starting in their teenage years. Everybody. But at a certain point it becomes too much to block the arteries and causes heart issues, whatever they might be – heart attack, heart failure or whatever. It's the same kind of process here."
Chris Nowinski, co-director of BU's Center for the Study of Traumatic Encephalopathy, disagreed strongly. He said Kutcher made the same argument to him when he visited BU last month.
"Of course you can have heart disease without having symptoms and having a heart attack, but when I go to the doctor, I get my blood pressure checked and cholesterol checked every time," Nowinski said with a laugh. "And I get a speech every time because the medical community is busting their butts to prevent those things and monitors them constantly. …
"To me, it seems incredibly simple. It's like saying, 'What's the big deal if your cholesterol's 300 if you're still walking around and breathing?' Because tomorrow you may not be."
Kutcher and Ruben Echemendia, the NHL's neuropsychological consultant, said no one has established scientifically what causes CTE, what effect CTE has and what the risk is. But BU defines CTE as a progressive degenerative disease that is triggered by repetitive head trauma, can begin months or years after the end of athletic involvement, and is associated with cognitive and behavioral problems.
Nowinski has his own comparisons.
"A better analogy to understand it is through cancer," Nowinski said. "I think there's two types based on what we're talking about here: lung cancer, breast cancer.
"Lung cancer's very similar. To get exposed, it's a voluntary exposure to a risk factor, smoking-related lung cancer. Even if you stop smoking, it starts a process [through] which an endpoint is cancer, and most people have no idea they have cancer until it's Stage 3 or 4. But we still care a hell of a lot about Stage 1 and 2, and we look for it and we attack it when we find it because we know … People at Stage 1 and 2 are fine. You cannot notice a difference. They're completely healthy, no changes, and then at 3 and 4 there's a good chance they're going to pass away from it. It destroys their life. …
"Breast cancer. Because we can now intervene with breast cancer, we screen the hell out of it. All the time, women are told to check, because if you catch it early, you could stop it. Twenty years go, everyone's caught at Stage 4, and it was too late. And now if you catch it at Stage 1, we have all sorts of interventions. If we had those sorts of interventions for CTE, we would be screening like crazy, too."
Nowinski said BU is working on diagnosing CTE in living people with the hope of treating it someday. He allowed that the rate of progression of CTE is unknown, but he insisted it has been established that the disease is progressive. How do we know?
"At this point you could say it's empirical experience, in that the youngest cases have very focal spots of it and as they died older it's inevitably more," Nowinski said. "And also we know that tau works that way in Alzheimer's – this [certain type of] tau can transmit itself from cell to cell. So it's kind of the Alzheimer's model and the empirical experience of, we're not looking at 18-year-old brains who have Stage 4 CTE and 80-year-old brains that have Stage 1."
So it's an educated opinion?
"It's more than educated opinion," Nowinski said. "It's an overwhelming amount of evidence, minus filling in every blank. …
"In public health, you eventually have to step away from the bench and say, we have to make a decision based on what we know. No one could look at all this stuff and say, 'We should wait longer just in case we find an 18-year-old who has Stage 4 CTE and dementia.' It's not going to happen."
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