Estimating the prevalence at death of CTE neuropathology among professional football players

A Decision-Analytic Approach to Addressing the Evidence About Football and Chronic Traumatic Encephalopathy

“…Note that some investigators have tried to quantify and/or adjust for this selection bias and generally concluded that even if the bias was at its extreme (i.e., if every single case of CTE in the cohort had already been enumerated because of bias), this lower-bound estimate of risk to football players would still be "significant" by all conventional meanings of that term. 6,51,52 The D0 hypothesis appears consistent with the Bieniek study results as well. The Bieniek study involves a convenience sample (involving an extant brain bank) and includes 66 former athletes and notably 198 participants in a comparator group (no exposure to contact sports), who were matched to the former athletes by age at death and by comorbid diseases.…”

“…First, although the case series (110 CTE diagnoses out of 111 former players autopsied) is clearly nonrepresentative, the numerator is already amply large for the minimum possible working-lifetime excess risk of CTE to be much larger than any legal, regulatory, or common-sense benchmark of "unacceptable risk." 6,51 Second, we observe that many of the arguments for ignoring the striking excess of CTE cases among those with RHI exposure (over a very low background rate in those without RHI exposure) are either illogical 5 (►Table 2 and the previous discussions of the irrelevance of anecdotal observations about single individuals "with [CTE or symptoms] but without [RHI or lesions]" and about individuals "without CTE/symptoms but with RHI or lesions"), self-negating (the argument that CTE lesions are not associated with symptoms contradicts the parallel argument that the case series only enrolled those with symptoms), and/or wholly unsupported (see, e.g., Randolph 34 and the argument that humans "must" have evolved resistance to the neurologic effects of RHI). g As the evidence supporting a serious CTE problem continues to accrue, the counterarguments are becoming increasingly desperate, it seems to us; in effect, 60 years after R.A. Fisher concocted his set of fallacious explanations for the excess lung cancer being observed in smokers (essentially, that there is a hidden genetic factor that causes both lung cancer and the craving to smoke 58 ), similar supernatural hypotheses are increasingly being proffered.…”

Meeting report: the 24th Annual Congress of the European College of Sports Science (ECSS) – 3-6 July 2019, Prague, Czech Republic

“…This estimate was supported in a subsequent analysis conducted by Zachary Binney and Kathleen Bachynski, published in Neurology [13]. These researchers showed (similarly) that, if 100% of the cases of CTE diagnosed post-mortem in former NFL players were being captured by the CTE brain bank (i.e.…”

First report the findings: genuine balance when reporting CTE

“…Given the history of NFLled attempts to downplay harm, a call for balanced reporting in this field can give undue credence to uncertainties. 6 A well documented history of what we term ignorance by design exists a particular disease, or without exposure but with the disease (as in lifelong smokers who died of food poisoning, or lung cancer in nonsmokers), are completely compatible with a true statistical or causal association between an expos ure and a disease. These logical falla cies, and others, are clouding the CTE literature.…”

“…These logical falla cies, and others, are clouding the CTE literature. 6 Researchers should be able to inter pret uncertain evidence differently without necessarily being accused of malfeasance. Stewart and colleagues 1 cite an essay 7 that con demns scientists for being "willing accomplices" 7 to mediafueled fraud, such as occurred with the debunked link between vaccines and autism.…”