Keith Olbermann opened his sports program Friday night discussing anecdotes and other stories suggesting that Lou Gehrig’s passing may not have been solely due to the disease – ALS – that also bears his name. Recent developments around the impact of concussions in sports (primarily, but not exclusively, American football) likely prompted Olbermann’s reassessment of interviews he’s conducted over the course of his career and additional anecdotes of baseball in the 1930s. Best to let the video tell the story.
The segment has attracted some attention, but it is only adding to a tale, not starting one. Olbermann did not – at least from my perspective – claim that he did not actually suffer from ALS. This was a debate a few years ago prompted by a study that found a different neurodegenerative disease in athletes who had accumulated head trauma and demonstrated symptoms close to those of ALS. The researchers could only distinguish between the neurodegenerative diseases via autopsy, and never did claim that Gehrig did not suffer from ALS. The problem was that popular accounts of the study used Gehrig as a known athlete with a similar disease and failed to make the distinction between conditions.
Confused? That’s quite understandable. In short, popular accounts of the study essentially missed a major point of the research – that there are a suite of neurodegenerative diseases that look similar, but have different mechanisms.
Coming back to Olbermann, his reporting and interviews around Gehrig’s conditions focus on accounts of what appear to be symptoms of accumulated head trauma. Gehrig did suffer several blows to the head during his career, which spanned 14 years. As his remains were cremated, the stories are all that exist to suggest that the same problems plaguing NFL players of today may have contributed to the early retirement and death of a baseball legend. What wasn’t mentioned, but could reasonably be inferred, is that Gehrig certainly wasn’t alone. The additive impact of the chronic brain injury and his ALS, along with his talent and endurance, make his story more notable.
It’s important to note here that in cases like this, where scientific assessments are conducted across a span of years, it’s really easy to conclude too much from available evidence. This goes beyond the old chestnut about correlation not being the same thing as causation. Controlling for bias is a challenge when the data is fresh and the subjects actively participating. When most of the evidence is at best second-hand, how can it be anything but incomplete? We all need to mind the line between reasonable conclusion and armchair speculation, as fuzzy as it can be.