An important study was recently published in the open access journal, PLOS ONE, analyzing the relationship between the severity of traumatic brain injury and anabolic steroid use.
In the Study, titled “Chronic Exposure to Androgenic-Anabolic Steroids Exacerbates Axonal Injury and Microgliosis in the CHIMERA Mouse Model of Repetitive Concussion” the authors noted that in about 20% of known Chronic Traumatic Encephalopathy (CTE) cases the subjects had a history of substance use including androgenic-anabolic steroids.
The authors questioned whether there was a connection between anabolic steroid use and severity of brain injury and conducted a study involving mice. Some of the mice received a cocktail of three anabolic steroids (testosterone, nandrolone and 17α-methyltestosterone) and were later exposed to two incidents causing traumatic brain injury.
The mice exposed to steroids exhibited significantly exacerbated axonal injury and microgliosis leading the authors to conclude that anabolic steroid use “can alter neuronal and innate immune responses to concussive TBI”
The full study is available by subscription and the abstract can be found here and is reproduced below –
Concussion is a serious health concern. Concussion in athletes is of particular interest with respect to the relationship of concussion exposure to risk of chronic traumatic encephalopathy (CTE), a neurodegenerative condition associated with altered cognitive and psychiatric functions and profound tauopathy. However, much remains to be learned about factors other than cumulative exposure that could influence concussion pathogenesis. Approximately 20% of CTE cases report a history of substance use including androgenic-anabolic steroids (AAS). How acute, chronic, or historical AAS use may affect the vulnerability of the brain to concussion is unknown. We therefore tested whether antecedent AAS exposure in young, male C57Bl/6 mice affects acute behavioral and neuropathological responses to mild traumatic brain injury (TBI) induced with the CHIMERA (Closed Head Impact Model of Engineered Rotational Acceleration) platform. Male C57Bl/6 mice received either vehicle or a cocktail of three AAS (testosterone, nandrolone and 17α-methyltestosterone) from 8–16 weeks of age. At the end of the 7th week of treatment, mice underwent two closed-head TBI or sham procedures spaced 24 h apart using CHIMERA. Post-repetitive TBI (rTBI) behavior was assessed for 7 d followed by tissue collection. AAS treatment induced the expected physiological changes including increased body weight, testicular atrophy, aggression and downregulation of brain 5-HT1B receptor expression. rTBI induced behavioral deficits, widespread axonal injury and white matter microgliosis. While AAS treatment did not worsen post-rTBI behavioral changes, AAS-treated mice exhibited significantly exacerbated axonal injury and microgliosis, indicating that AAS exposure can alter neuronal and innate immune responses to concussive TBI.
Update – This article has been republished at MixedMartialArts.com where a forum member helpfully points to this 2013 study which concludes that long-term high-dose anabolic-androgenic steroids exposure may cause cognitive deficits, notably in visuospatial memory even without exposure to head trauma.