CTE: Media Continues To Be Ahead Of Science
The prevailing media narrative is that concussions or repetitive subconcussive blows “cause” chronic traumatic encephalopathy (CTE), that CTE “causes” former athletes to commit suicide, and such causal links are proven scientific fact.
The prevailing media message, says Scottish neuropsychiatrist Alan Carson in a 2017 editorial commentary in a British medical journal, is that “concussion is a dangerous condition that causes” CTE, accompanied by mood change, irritability, and suicidal behavior which develops over time into a neurodegenerative disorder and death.” What follows is increasing alarm, accompanied by the suggestion that CTE is not just a disorder of elite athletes but a problem for youth sport and that even heading a soccer ball may cause dementia, “a terrifying prospect for parents trying to decide whether to allow their children to participate in sports.”
It thus may come as a surprise to many that, despite widespread media coverage and speculation regarding the late-life or post-retirement risks of cognitive impairment or neurodegenerative disease such as CTE in athletes who engaged in sports involving repetitive blows to the head and high concussion risk, and assertions that CTE causes them to be at high risk of suicide, there have been virtually no peer-reviewed, well-designed scientific studies that establish, much less quantify, such risks.
The problem is that, while some scientists who have in the past appeared most willing to push the envelope by arguing that such a cause-and-effect relationship exists in public, may be exercising more caution in reporting the results of their research in scientific journals, that caution is often be lost in translation when their research is reported by the mainstream media.
No consensus on causation
Rejecting the blanket conclusion that there is a definitive causal and effect connection between repetitive head trauma and CTE, most peer-reviewed scientific papers, including the most recent quadrennial international consensus statement on concussion in sport (“Berlin 2016”), caution that, while there is clearly a link between CTE and concussions and/or exposure to repetitive head trauma in contact and collision sports, the precise relationship is not yet known.
The conclusion by the head injury researchers in the Zurich 2012 statement put it succinctly: a “cause-and-effect relationship has not yet been demonstrated between CTE and [sports-related concussions] or exposure to contact sports. As such, the notion that repeated concussion or subconcussive impacts cause CTE remains unknown.”
The view that the football=dementia meme is scientifically premature has long been espoused by some researchers, including Christopher Randolph, PhD. a now retired professor at Loyola University in Chicago. In a 2013 study of retired NFL players — who largely comprise the highly limited, self-selected universe from which the case studies of brains showing the presence of CTE have been drawn (what scientists call a “convenience sample”), and who the media have widely reported as being at high risk of CTE — Randolph lamented that “the media attention to this issue continues to far outweigh any meaningful results from sound experimental science.”
Randolph found that, when compared with healthy controls and with non-athlete patients with a clinical diagnosis of mild cognitive impairment (MCI) commonly presumed to reflect the earliest stage of Alzheimer’s disease, the patterns of impairments of the retired NFL players in the study were virtually identical to those exhibited by non-athletes with MCI. The finding lead him and his colleagues to conclude that CTE might not be a distinct neurodegenerative disorder at all.
Randolph’s 2013 study appeared to lend support to his theory, first proposed in a 2009 paper, that a long history of repetitive head trauma in contact sports does not cause CTE, but might eventually result in a diminished cerebral reserve leading in some unknown percentage of cases to an earlier-than-normal expression of other common, age-related neurodegenerative diseases,such as Alzheimer’s Disease (AD) and Parkinson’s (PD). His theory was that the ways in which such diminished cerebral reserve would be expressed (e.g. mild cognitive impairment (MCI), AD, PD, ALS) would not differ from individuals with those diseases who lacked such a history of head trauma, which is precisely what his 2013 study suggests. A 2015 meta-analysis of 153 published cases of CTE, and a 2017 study by Canadian researchers (see discussion below) suggests much the same.
