Anabolic steroids don't appear to contribute to degenerative brain disease caused by repeated head trauma in athletes, according to a study in the January issue of Neurosurgery, official journal of the Congress of Neurological Surgeons. The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.
The experimental findings do not support the theory that steroid use by athletes plays a role in the long-term damaging effects of mild traumatic brain injury (MTBI). The lead author was Dr. James D. Mills of West Virginia University, Morgantown.
No Difference in Effects of Brain Trauma with vs without Steroids
Dr. Mills and colleagues designed an experiment to determine whether treatment with anabolic steroids makes any difference in the effects of brain trauma in rats. It has been suggested that steroids may contribute to the abnormalities seen in chronic traumatic encephalopathy (CTE): a progressive neurodegenerative disease linked to concussions and other forms of MTBI. In recent years, a growing number of cases of CTE have been identified in athletes, especially football players.
Use of anabolic steroids has increased dramatically in recent decades, mainly among athletes seeking a competitive advantage. Because athletes are also at high risk of sustaining concussions or MTBI, it's possible that steroid use could be a factor in the development CTE.
The researchers used a standard technique to induce traumatic brain injury in rats, some of which were treated with anabolic steroids before and after injury. Brainstem specimens were analyzed to compare levels of a protein called beta-amyloid precursor protein (APP): an indicator of brain cell damage caused by MTBI.
The results showed no difference in responses to brain injury between rats that were and were not treated with steroids. Both groups of animals had similar elevations in AAP level. In a comparison group of rats that were not subjected to brain injury, there was no difference in APP levels with versus without steroid treatment.
Typically occurring in former professional athletes years after retirement, CTE is associated with a wide range of mental, emotional, and physical problems. The brains of patients with CTE show a distinct pattern of abnormalities for which brain trauma is the only known cause.
The new results cast doubt on the theory that anabolic steroid use could be a cause or contributing factor to the development of CTE. While acknowledging the limitations of their animal experiments, Dr. Mills and coauthors write, "[W]e see no adverse effect or causative role of anabolic steroid administration on the brain following MTBI with the use of APP counts as a marker for anatomic injury." Rather, they point to a growing body of clinical research strongly suggesting that CTE risk is "most likely related to exposure to repetitive MTBI with a tendency toward a genetic predisposition."