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A tragic case
Todd Ewen was a National Hockey League (NHL) ‘tough guy’ who accumulated over 1900 penalty minutes in 518 games across 12 NHL seasons. He recently committed suicide after bouts of depression at the age of 49. Before an autopsy had been performed, the media pre-emptively wrote about how his depression and suicide were most likely the result of a career in the NHL, repetitive head trauma and the inevitable onset of chronic traumatic encephalopathy (CTE).1 Ewen himself was convinced he had developed CTE, as his wife recalled him being terrified by the thought of a future living with a neurodegenerative disease.2 Ewen's brain was examined by neuropathologists at the University of Toronto—they found no evidence of CTE. So we ask, how did a professional athlete who had treatable depression, come to believe that he had an untreatable condition and committed suicide?3
The availability cascade, headline news and double standards
The public's perception of sport-related concussion (SRC) and CTE is likely not based on the totality of empirical data, but rather on highly publicised and emotionally charged events. CTE is not a new diagnosis, as it was first described almost a century ago in 1928.4 However, only recently has CTE come to the forefront of public attention because of the highly publicised cases of National Football League (NFL) players presenting with this disease posthumously. As a result, there is a presumption that a direct causal link between repetitive head contact and CTE exists. ‘Historical biases’ and ‘the Semmelweis effect’ may cause the media to ignore non-significant findings and any new evidence that contradicts this established ‘norm’. Deemed ‘the availability cascade’, social pressures can cause individuals to believe, endorse and propagate this one-sided, biased perception.
CTE is certainly a neuropathological diagnosis associated with and observed posthumously in some athletes and individuals who have endured repetitive head contact.5 However, we do not know what the true aetiology/mechanisms are; how many will develop or have the disease; if there are other relevant comorbid factors at play including genetics, cardiovascular health and substance abuse; or even the clinical presentation of this disease. For instance, are there patients with CTE who are asymptomatic? And to what degree can symptoms such as depression be disentangled from general mood disorder and/or concomitant neurodegenerative diseases?
Despite knowledge gaps, media may have propagated an agenda of one-sided headline news and a sensationalised state of fear. Researchers from the Department of Veterans Affairs and Boston University released data to PBS's FRONTLINE, indicating that a staggering 96% of NFL players they examined had CTE.6 FRONTLINE reported ‘several caveats’, including that “players who have donated their brains for testing suspected that they had the disease while still alive, leaving researchers with a skewed population to work with”. Yet, the piece then proceeded to downplay the effects of ‘selection bias’ on the reported prevalence rate in the following paragraph. When other scientists in the field publish contrary research, and explain potential ‘selection bias’,7 the media ‘up-play’ these flaws and become very critical of the research, and also the researchers and anyone associated.8 As a result, those who challenge the ‘status quo’ and demand that further study is needed are labelled as conspiring ‘deniers’ or ‘shills’ with other vested interests, trying to confuse the public and conflate the issue.
Moving forward and repairing the disconnect
We propose a three-pronged approach to repairing the disconnect between the science and the media with regard to SRC and CTE. First, as researchers and members of the media, we must acknowledge our own cognitive biases: ‘Belief bias’ and ‘the backfire effect’ cause us to hold tight to the most ‘common-sense conclusions’ and our own beliefs, rather than reconciling conflicting or contrary evidence; ‘illusion of validity’ causes us to believe that the quantity of research generated is equally as important as the quality of evidence garnered; and finally, ‘bias blind spot’ is the tendency to see oneself as less biased than others. Acknowledging our own cognitive biases will allow us to entertain and reconcile the empirical evidence of SRC in its totality. Second, as medical and research professionals, it is our job to disseminate the science to the media. We should aim to spend more time educating the media as well as encouraging their attendance and active participation in large academic meetings or conferences. Undoubtedly, the media play a crucial intermediary role in providing information to the public. Third, collaboration within the field is a critical step in progressing the science further and having a more informed populous. As opposed to one-sided press releases or sharing limited results with the media, writing letters and responses to journal editors or participating in back-and-forth debates at large academic conferences will promote cordial discourse as opposed to harsh division and polarisation within the field.
Twitter Follow Andrew Kuhn at @kuhnaw
Contributors AWK and SLZ conceived the article. AWK, SLZ, AMY-K and ZYK contributed by drafting and editing the article.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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