Four new scientific papers[1-4] are adding to the growing chorus of researchers pouring cold water on the now common assumption in the media and general population that contact sports causes CTE, and that CTE causes those with the disease to commit suicide.
Circular reasoning
In the first, reported in the British Journal of Sports Medicine,[1] a leading concussion researcher, Grant Iverson, MD, of the Department of Physical Medicine and Rehabilitation at the Harvard Medical School, finds the "insufficient scientific evidence" to support a finding of the existence of a causal relationship between CTE and suicide in former athletes, and that concluding that CTE caused suicidality was "premature" because it was based on a small number of individuals who completed suicide.
The reason, he says, is because "the relevant research has simply not been performed." In fact, notes Iverson, "according to the only published epidemiological data until now, NFL players are at decreased risk, not increased risk, for completed suicide relative to the general population."
Finding evidence of CTE in the brains of former athletes who complete suicide, writes Iverson, "is a provocative but not statistically compelling source of evidence. The finding a causal link in individual cases represents, says Iverson, "circular reasoning" or what philosophers call petitio principii: begging the question by assuming without proof a proposition which requires it.
Risk factors for suicide
Among the many known risk factors for suicide Iverson identifies are:
- depression (long considered the psychiatric disorder most associated with suicide, research actually suggests that, while thinking about suicide (i.e. suicidal ideation) is predicted by depression, suicide plans and attempts are more strongly associated with anxiety/agitation (eg. post-traumatic stress disorder) and poor impulse control (eg, drug misuse);
- life stress: major interpersonal stessful life events might precipitate suicide attempts in people with alcohol problems;
- difficult childhood (e.g. physical abuse, sexual abuse, domestic violence)
- physical illnesses
- intepersonal family conflict
- personality disorders
- impulsivity and aggression
- hopelessness
- previous suicide attempts
- for adults over 50:
- depression
- aggression
- limited social connectedness
- poor physical health
Because a mature body of evidence outside sports thus suggests that the causes of suicide are "complex, multifactorial, and difficult to predict in individual cases," and given that there were just nine reported deaths by suicide in former NFL players between 1960 and 2007, and six reported suicides in the past 2 years, "it is essential," says Iverson, "to carefully investigate the diverse range of risk factors for suicidality in former athletes - and not adopt a singular mechanistic assumption about [CTE] as the primary explanation."
This is not to say, as Iverson notes, that former athletes are not likely at increased risk of suicidal ideation and completed suicide as a result of a number of factors:
- steroid use: a substantial minority of retired NFL players admitted in a recent survey[6] to a history of anabolic steroid use during their playing career, with one in five players from the 1980s reporting taking steroids. Steroid use is associated with:
- greater risk for musculoskeletal injuries
- increased lifetime risk for back pain and depression
- increased future risk for suicide in former Swedish wrestlers, power lifters, Olympic lifters, and those in track and field throwing events,[7] with one small Finnish study reporting a possible connection between steroid use and future suicide.[8]
- chronic pain: 8 out of 10 former NFL players in one phone survey[9] reported moderate or severe problems with chronic pain. Studies show that patients seeking treatment for chronic pain have high rates of depression, and there is also evidence that patients with chronic pain are at increased risk of suicidal ideation and of suicide.
- misuse of prescription opiads: of the half of former NFL players who used prescription narcotic pain medication during their playing careers, 7 in 10 reported misusing them, and those with such a history were significantly more likely to continue misusing them after retirement; such misuse was significantly associated with greater levels of pain, self-reported history of undiagnosed concussions, and current heavy drinking.
- life and financial stress: former NFL players with depression, and especially those with depression and chronic pain, are much more likely to report life stress and financial difficulty than former players without depression.
Iverson concludes that additional research is needed to determine the extent to which CTE is a possible factor associated with suicide. Until then, he says, "researchers and clinicians are encouraged to be prudent, circumspect and critical in their approach to interpreting the strongly presented causal relationship between ... CTE and suicide that is discussed frequently in the media and increasingly in the public literature."
Jumping to conclusions
In the second, published in the journal Behavioral Sciences and the Law, [2] scientists at the University of Colorado School Medicine conduct a state-of-the-science review of CTE, explore the evidence for links between traumatic brain injury (TBI), CTE and catastrophic clinical events such as suicide, and highlight the complexity of specifically attributing suicide to CTE, Like Iverson, they urge caution in jumping to conclusions on the basis of preliminary case study autopsies.
While saying it is not their intention to "dismiss the science of CTE, or to discourage ongoing efforts to mitigate the frequency of concussion/TBI sustained by athletes, military personnel, and/or civilians," Hal Wortzel, MD, and his colleagues recommend that clinicians, scientists, and the public remain "circumspect" about the science of CTE.
Like Iverson, they call for more research in this area - especially well-designed, prospective, longitudinal, multicenter, large-population studies to determine the consequences of concussions on long-term neuropsychiatric health.
They acknowledge that "it simply makes good clinical sense to continue practices to minimize the number of concussions sustained and that allow for adequate recovery after any concussion" while awaiting the results of such studies. At the same time, however, Wortzel and his colleagues state that it is "essential to avoid embracing preliminary results derived from relatively small case numbers and methodologically problematic studies as undisputed medical fact, and to allow such results to redirect clinical practice away from established standards."
Wortzel thus says a concerted effort is needed to educate medical professionals and the public at large regarding the state of the science of mTBI and CTE in order to "correct emerging misconceptions regarding the natural history of TBI, and mild TBI in particular," so as to avoid "catastrophizing" mTBI, mitigate the "collective anxiety" that has been generated by widespread media reports blaming CTE and suicide on a history of head trauma, and reduce the likelihood that outcomes after mTBI will be actually be made worse as a result of the media frenzy around CTE.
Case studies: weakest form of scientific research
In the third commentary, published in the journal Neuropsychological Review,[3] Christopher Randolph, PhD, of Loyola University in Chicago, a leading skeptic about the supposed link between CTE and contact sports, reviews the history of so-called "classic" CTE in boxers, the literature on "modern" CTE (case studies from 2005 forward), mainly in American football players, explores the sampling and methodological issues that, he says, prevent any firm conclusions about the association between athletic head trauma and neurodegenerative diseases such as CTE being drawn, and calls, like Iverson and Wortzel, for more carefully-controlled epidemiological and prospective studies to overcome current limitations in this research and stimulate further research.
"Much more research needs to be undertaken in order to better understand the modern concept of CTE," Randolph writes. We need to "move beyond case reports or samples of convenience in defining CTE, from both a clinical and pathological basis" because they are "the weakest of all scientific methods, best suited for discovery and for launching hypotheses rather than confirming them."
Unanswered questions
Finally, commenting in the British Journal of Sports Medicine on a systematic review of the literature on CTE in sport[5] published in the same issue of the journal, Charles Tator, MD, of the Division of Neurosurgery at the University of Toronto, notes the "significant advances" over the past 10 years in understanding CTE that have allowed the sports community to understand that the issue of brain degeneration as a consequence of repetitive concussion is not confined to boxers but applies at least to hockey, football, wrestling, and rugby.[4]
Tator emphasizes, however, says that there are many questions to be answered, among them:
- the percentage of concussed athletes that will develop CTE
- the exact relationship between concussion and brain degeneration
- how many concussions are required to cause brain degeneration
- whether subconcussive blows lead to the same neurological deficits and pathological changes as concussive blows
- whether it is possible to recognize clinical precursors to CTE, such as post-concussion syndrome
- whether the changes in the brain resulting from repetitive concussions are specific to concussions or are similar to degenerative changes that occur as a result of normal aging or diseases of aging, such as Alzheimer's, dementia, and Parkinson's disease
- how many non-concussed athletes or non-athletes will have any of the changes in the brain, such as tau protein deposits, considered specific markers for CTE.
Like Iverson, Wortzel, and Randolph, Tator says longitudinal studies of large number of at-risk athletes are "essential."
1. Iverson GL. Chronic traumatic encephalopathy and risk of suicide in former athletes. Br J Sports Med. 2013; doi:10.1136/bjsports-2013-092935 (epub October 31, 2013).
2. Wortzel HS, Brenner LA, Arciniegas DB. Traumatic Brain Injury and Chronic Traumatic Encephalopathy: A Forensic Neuropsychiatric Perspective. Behav. Sci. Law; 2013; doi:10.1002/bsl.2079 (epub on line).
3. Karantzoulis S, Randolph C. Modern Chronic Encephalopathy in Retired Athletes: What is the Evidence? Neuropyschol Rev 2013; doi:10.1007/s11065-013-9243-4 (epub November 22, 2013)
4. Tator CH. Chronic traumatic encephalopathy: How serious a sports problem is it? Br J Sports Med. 2013; doi:10.1136/bjsports-2013-093040 (epub November 22, 2013).
5. Gardner A, Iverson G, McCrory P. Chronic traumatic encephalopathy in sport: a systematic review. Br J Sports Med. 2013; doi: 10.1136/bjsports-2013-092646 (epub June 26, 2013).
6. Horn S, Gregory P, Guskiewicz KM. Self-reported anabolic steroid-androgenic steroids use and musculoskeletal injuries: findings from the center for the study of retired athletes survey of retired NFL players. Am J Phys Med Rehabil 2009;88:192-200.
