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Question clinique
Are former professional soccer players at increased risk for neurodegenerative disease?
L’Essentiel
Being a former professional soccer player in Scotland is associated with a greater risk of having a neurodegenerative disease (especially Alzheimer disease) listed on their death certificate than matched control patients, as well as a greater likelihood of having been prescribed medication for dementia. The absolute rates were 2.9% versus 1.0% over a median of 18 years (number needed to play pro soccer to harm = 52). Limitations include attribution bias due to inaccurate assignment of the cause of death on death certificates and the fact that all of the players were men. We also don't know if playing recreational soccer carries the same increase in risk or if delaying implementation of heading until adolescence makes a difference 2b
Référence
Plan de l'etude: Cohort (retrospective)
Financement: Foundation
Cadre: Population-based
Sommaire
The association between participation in US football and chronic traumatic encephalopathy is well established. This study looked at real football (what Americans call soccer) in which players routinely use their heads to strike a ball that has flown 40 or 50 meters, and not infrequently collide heads as they compete for the ball. The authors identified a database of former Scottish professional soccer players and merged it with electronic health records that included the cause of death and any medications prescribed prior to death. A total of 7676 players were identified who could be matched to the health data, and those players were matched on a 1-to-3 basis to control patients from the general population on the basis of age, sex, and socioeconomic status (called social deprivation in the United Kingdom). Patients entered the study at age 40, and were followed up for a median of 18 years. A fairly sophisticated analysis was performed, beginning with a Cox proportional hazards regression. If the proportional hazards assumption was not met because risk varied by period (for example, the survival curves crossed), a model was created that calculated hazard ratios during different follow-up periods. Former players had lower all-cause mortality (hazard ratio [HR] 0.80; 95% CI 0.80 - 0.93), but the proportional hazards assumption wasn't met: Their mortality was lower before age 70 years, but higher after age 70. The likelihood that any neurodegenerative disease was listed as the primary cause of death was significantly higher in former players than in control patients (1.7% vs 0.5%). After adjusting for competing causes of death, the risk remained (HR 3.5; 2.1 - 5.6). Similarly, any neurogenerative disease was listed as either the primary or a contributing cause of death more often in former players (HR 3.5; 2.7 - 4.6). The increase in risk was greatest for Alzheimer disease (HR 5.1; 2.9 - 8.8) and lowest for Parkinson disease (HR 2.1; 1.2 - 4.0). Former players were also more likely to have received medication for dementia than matched control patients (odds ratio [OR] 4.9; 3.8 - 6.3). Although there were trends toward less neurodegenerative disease as a cause of death in goalkeepers than in other players, these were not statistically significant. Goalkeepers, however, were less likely to have received dementia medications (OR 0.41; 0.19 - 0.89).
Reviewer
Mark H. Ebell, MD, MS
Professor
University of Georgia
Athens, GA