5 FAQ that don’t challenge CTE causation

By Adam Finkel, ScD & Chris Nowinski, PhD

The five questions below about repetitive head impacts (RHI) and CTE are based on natural observations that are frequently made by sports organizations, former athletes, and even some physicians.

Unfortunately, they have been inappropriately used by doctors associated with sports leagues, including NFL advisors and NFL- and NHL-sponsored neuropsychologists, to trivialize CTE or to attempt to refute that RHI causes CTE, and that CTE causes dementia.

We wrote this blog to clear up any confusion and to accompany our recent publication on CTE causation, Applying the Bradford Hill Criteria for Causation to Repetitive Head Impacts and CTE.

It’s important to note these five questions do not provide actual counterevidence, only anecdote. However, none of the observations below, even if they were supported by data rather than anecdote, cast any doubt on the conclusions that RHI causes CTE and that CTE is a grave disease.  




Scientific Answer


“What about people who have had substantial exposure to RHI but never developed CTE?”

The very definition of “risk” ensures that some individuals will escape the consequences of risky exposure. Many people smoke cigarettes and never develop lung cancer.  “Risk” and “certainty” are entirely different concepts.


“What about people who developed CTE but had never sustained any RHI?”

Even if there is another path to CTE (currently, there is no evidence for another cause), most environmental or occupational diseases have multiple causes. There are many causes of lung cancer other than cigarette smoking. The fact that radon gas can cause lung cancer says nothing about whether cigarettes cause lung cancer.


“What about people who were found with CTE but never manifested symptoms?”

Many diseases have variable presentations. Consider pre-symptomatic Alzheimer’s disease pathology, precancerous lesions, etc.  The fact that some people may be pre-symptomatic or have a seemingly stable, mild, or slow-moving form of a disease says nothing about others whose disease can progress rapidly and severely.


“What about those who had symptoms but were found not to have had CTE?”

Many symptoms are nonspecific. Memory problems, depression, etc. have multiple causes. It doesn’t mean that CTE can’t also cause them.


“Why do we talk about children and CTE when no children under 17 have been diagnosed with CTE?”

For the same reasons we prevent children from smoking even if we’ve never seen a 13-year-old with lung cancer.

First, there is a known lag between the exposure and the disease. At some point, CTE has been set in motion, even though the victim may not have the diagnostic lesion for years, or symptoms for decades. 

Second, the science thus far says, similar to smoking and lung cancer, that the more exposure to RHI, the more likely you are to develop CTE, regardless of when that RHI occurred

Sometimes analogy can be helpful. Everyone has known for decades that smoking causes lung cancer.  Imagine if someone told you

“Smoking doesn’t cause lung cancer, because…”

  • I heard of someone who smoked heavily and didn’t get lung cancer…
  • I heard of someone who got lung cancer but never smoked…


“Lung cancer doesn’t cause serious symptoms, because…”

  • I heard of someone whose lung cancer was mild…
  • I heard of someone who was short of breath but didn’t have lung cancer...


"It’s OK for that child to smoke two packs-a-day because…"

  • I heard they plan to stop by age 18.

Would any of these statements change your mind about whether cigarette smoking causes lung cancer? Of course not. It’s not surprising to hear these statements from some physicians, neuropsychologists, or researchers if they don’t have training in public health. But public health professionals, trained in interpreting evidence, never offer these statements to doubt causation.


Adapted by Nowinski CN & Finkel AM from Brand KP, Finkel AM. A Decision-Analytic Approach to Addressing the Evidence About Football and Chronic Traumatic Encephalopathy. Semin Neurol. 2020 Aug;40(4):450-460.

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